CLEC10A
| CLEC10A | |||
|---|---|---|---|
| Identifiers | |||
Gene ontology | |||
| Molecular function | |||
| Cellular component | |||
| Biological process | |||
| Sources:Amigo / QuickGO | |||
Ensembl | |||||||||
|---|---|---|---|---|---|---|---|---|---|
| UniProt | |||||||||
| RefSeq (mRNA) | |||||||||
| RefSeq (protein) | |||||||||
| Location (UCSC) | Chr 17: 7.07 – 7.08 Mb | Chr 11: 70.05 – 70.06 Mb | |||||||
| PubMed search | [3] | [4] | |||||||
| View/Edit Human | View/Edit Mouse |
C-type lectin domain family 10 member A (CLEC10A) also designated as CD301 is a
Function
Generally, C-type lectins bind carbohydrate moieties usually in the presence of Ca2+ and have diverse functions, such as cell adhesion, cell-cell signalling, glycoprotein turnover, and roles in inflammation and immune response.[8]
CLEC10A is a type II transmembrane protein (passing one time through the membrane and oriented with the N terminus inward) that induces endocytosis after ligand binding. To release the ligand in the endosome, participating Ca2+ ions have to be unbound first. This leads to a significant increase in cytoplasmic Ca2+ concentration.[7]
CLEC10A binds most strongly to
CLEC10A has also been shown to bind GalNAc in the teichoic acid of the Staphylococcus aureus cell wall and the surface of parasites.[11][12]
CLEC10A is expressed by dendritic cells that differentiate from monocytes recruited to inflammatory environments.[13]
CD45 contains a Tn antigen in exon B. CD45 has 3 important exons (4,5,6), that are designated A,B,C. Isoforms of CD45 are labeled depending on the presence of these exons. CLEC10A can for example bind CD45RB or CD45R, which is shorthand for CD45RABC. Binding causes attenuation of T cell activity, apoptosis, and immunosuppression. However, active T cells express shorter isoforms of CD45 (CD45RO, CD45RA) that lack exon B.[7]
CLEC10A signalling induces
In cancer research, CLEC10A expression was found to both improve[14][15][16] and worsen[17] survival.
In animal models, deficiency of the orthologue to CLEC10A, Mgl1 is associated with worse outcomes in infection and excessive inflammation.[18]
References
- ^ a b c GRCh38: Ensembl release 89: ENSG00000132514 – Ensembl, May 2017
- ^ a b c GRCm38: Ensembl release 89: ENSMUSG00000000318 – Ensembl, May 2017
- ^ "Human PubMed Reference:". National Center for Biotechnology Information, U.S. National Library of Medicine.
- ^ "Mouse PubMed Reference:". National Center for Biotechnology Information, U.S. National Library of Medicine.
- S2CID 25597354.
- PMID 29755453.
- ^ PMID 32650396.
- S2CID 7084402.
- S2CID 32172457.
- PMID 23507963.
- PMID 31219660.
- PMID 15802303.
- PMID 29967419.
- PMID 31455323.
- PMID 29665849.
- S2CID 242193292.
- PMID 32019882.
- PMID 26912318.
Further reading
- Bonaldo MF, Lennon G, Soares MB (September 1996). "Normalization and subtraction: two approaches to facilitate gene discovery". Genome Research. 6 (9): 791–806. PMID 8889548.
- van Vliet SJ, Steeghs L, Bruijns SC, Vaezirad MM, Snijders Blok C, Arenas Busto JA, et al. (October 2009). Seifert HS (ed.). "Variation of Neisseria gonorrhoeae lipooligosaccharide directs dendritic cell-induced T helper responses". PLOS Pathogens. 5 (10): e1000625. PMID 19834553.
- Iijima M, Tomita M, Morozumi S, Kawagashira Y, Nakamura T, Koike H, et al. (October 2009). "Single nucleotide polymorphism of TAG-1 influences IVIg responsiveness of Japanese patients with CIDP". Neurology. 73 (17): 1348–1352. S2CID 207116106.
External links
- Human CLEC10A genome location and CLEC10A gene details page in the UCSC Genome Browser.
This article incorporates text from the United States National Library of Medicine, which is in the public domain.